Готові списки джерел за темами / Universal definition of myocardial infarction

Добірка наукової літератури з теми "Universal definition of myocardial infarction"

Автор: Grafiati
Опубліковано: 28 вересня 2022
Оновлено: 28 січня 2023

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  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій

Статті в журналах з теми "Universal definition of myocardial infarction":

1

Thygesen, K., J. Alpert, and H. White. "UNIVERSAL DEFINITION OF MYOCARDIAL INFARCTION." Rational Pharmacotherapy in Cardiology 4, no. 5 (January 1, 2008): 91–105. http://dx.doi.org/10.20996/1819-6446-2008-4-5-91-105.

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2

Parkhomenko, O. M. "Universal definition of myocardial infarction." Ukrainian Journal of Cardiology 28, no. 6 (February 1, 2022): 41–68. http://dx.doi.org/10.31928/1608-635x-2021.6.4168.

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The document is based on the Fourth Universal Definition of Myocardial Infarction, developed jointly by experts from the European Society of Cardiology (ETC) / American College of Cardiology (ACC) / American Heart Association (AHA) and the World Heart Federation (WFF) working group.
3

Thygesen, Kristian, Joseph S. Alpert, and Harvey D. White. "Universal Definition of Myocardial Infarction." Circulation 116, no. 22 (November 27, 2007): 2634–53. http://dx.doi.org/10.1161/circulationaha.107.187397.

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4

Hall, A. S., and J. H. Barth. "Universal definition of myocardial infarction." Heart 95, no. 3 (November 25, 2008): 247–49. http://dx.doi.org/10.1136/hrt.2008.147223.

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5

Thygesen, Kristian, Joseph S. Alpert, and Harvey D. White. "Universal Definition of Myocardial Infarction." Journal of the American College of Cardiology 50, no. 22 (November 2007): 2173–95. http://dx.doi.org/10.1016/j.jacc.2007.09.011.

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6

Thygesen, Kristian, Joseph Alpert, Allan Jaffe, Maarten Simoons, Berbard Chaitman, and Harvey White. "Third universal definition of myocardial infarction." Srce i krvni sudovi 32, no. 4 (2013): 29–46. http://dx.doi.org/10.5937/siks1301029t.

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7

Singh Joy, Subhashni D. "Updated Universal Definition of Myocardial Infarction." AJN, American Journal of Nursing 113, no. 2 (February 2013): 69. http://dx.doi.org/10.1097/01.naj.0000426696.49696.ec.

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8

Thygesen, Kristian, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman, Harvey D. White, Kristian Thygesen, et al. "Third universal definition of myocardial infarction." European Heart Journal 33, no. 20 (August 24, 2012): 2551–67. http://dx.doi.org/10.1093/eurheartj/ehs184.

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9

Thygesen, Kristian, Joseph S. Alpert, and Harvey D. White. "Third universal definition of myocardial infarction." Revista Portuguesa de Cardiologia (English Edition) 32, no. 7-8 (July 2013): 643–44. http://dx.doi.org/10.1016/j.repce.2013.10.002.

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10

Locca, Didier, Chiara Bucciarelli-Ducci, Giuseppe Ferrante, Alessio La Manna, Niall G. Keenan, Agata Grasso, Peter Barlis, et al. "New Universal Definition of Myocardial Infarction." JACC: Cardiovascular Interventions 3, no. 9 (September 2010): 950–58. http://dx.doi.org/10.1016/j.jcin.2010.06.015.

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Дисертації з теми "Universal definition of myocardial infarction":

1

Jacquin, Laurent. "Déséquilibre d’oxygénation et lésions myocardiques aiguës : approche clinique en service d’accueil des urgences." Thesis, Lyon, 2021. https://n2t.net/ark:/47881/m6736qrr.

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Dans ce travail de thèse, nous nous sommes intéressés en première partie aux critères de déséquilibre d’oxygénation impliqués dans la survenue d’un infarctus de type 2. Nous avons exploré chez 610 patients l’association entre les paramètres de ces critères et la survenue de lésions myocardiques aiguës, et d’infarctus de type 2, ainsi que la relation entre ces paramètres et l’extension de l’atteinte du myocarde. Nos résultats ne montraient pas de lien entre l’amplitude du déséquilibre d’oxygénation et la survenue de lésions myocardiques aiguës. Il n’y avait également pas de corrélation avec l’importance de ces lésions. Nous n’avons donc pas pu définir de seuils restrictifs stricts considérés comme facteur de stress myocardique significatif. Dans la deuxième partie, nous avons comparé le devenir à court terme et à distance des patients admis avec une condition de déséquilibre d’oxygénation en fonction de la présence d’une lésion myocardique, ou d’un infarctus de type 2, et évaluer l’association de ces entités pathologiques avec la mortalité et les évènements cardiovasculaires. Dans cette population de 824 patients, la survenue de lésions myocardiques aiguës non-ischémiques ou d’infarctus de type 2 conduisait à une mortalité hospitalière élevée à plus de 20% et y était significativement associée après ajustement sur les caractéristiques des patients. A plus long terme chez les survivants, le devenir était dépendant des comorbidités sans implication de la survenue de ces lésions myocardiques initiales, avec des taux de mortalité de 27 à 35 % et d’évènements cardiovasculaires de 23 à 40%. Nous avons proposé de confronter ces résultats dans une autre étude, menée prospectivement, avec un suivi standardisé à 6 mois des patients admis en déséquilibre d’oxygénation, dont nous détaillons la méthodologie. Cette cohorte est constituée de 670 patients dont l’analyse des données est en cours. Enfin, dans une troisième partie, nous nous sommes focalisés sur les 675 personnes âgées, qui représente plus de 80% de notre cohorte, pour déterminer les facteurs associés à la survenue de ces lésions myocardiques et infarctus de type 2 en fonction des classes d’âge. Nous avons retrouvé des profils de patients très dépendants de ces classes, liés aux évolutions épidémiologiques du vieillissement. L’individualisation des infarctus de type 2 au sein des lésions myocardiques aiguës n’était cependant pas évidente, de même que l’impact sur la mortalité qui reposait essentiellement sur le poids des comorbidités
In the first part, we were interested in the criteria of oxygen supply/demand imbalance involved in the occurrence of a type 2 infarction. We explored in 610 patients the association between the parameters of these criteria and the occurrence of acute myocardial injury and type 2 infarction, as well as the correlation between these parameters and the extent of myocardial injury. Our results did not show any association between the importance of oxygen mismatch and the occurrence of acute myocardial injury. There was also no correlation with the magnitude of such injury. Therefore, we could not define strict restrictive thresholds that could be considered a significant myocardial stressor. In the second part, we compared the short-term and the long-term outcomes of patients admitted with an oxygen supply/demand imbalance condition according to the presence of myocardial injury or type 2 infarction and assessed the association of these pathological entities with mortality and major cardiovascular events. In this population of 824 patients, the occurrence of myocardial injury or type 2 infarction led to high in-hospital mortality of more than 20% and was significantly associated with it after adjustment for patient characteristics. In the follow-up of survivors, the outcome was dependent on comorbidities without the involvement of the occurrence of these initial myocardial injuries, with mortality rates of 27 to 35% and major cardiovascular events of 23 to 40%. We proposed to compare these results in another study, conducted prospectively, with a standardized 6-month follow-up of patients admitted for oxygenation failure, the methods of which are detailed here. This cohort consists of 670 patients whose data are currently being analyzed. Finally, in the third part, we focused on the 675 elderly patients, who represent more than 80% of our cohort, to determine the factors associated with the occurrence of these myocardial injuries and type 2 infarction according to age classes. We found very dependent patient profiles in these classes, linked to the epidemiological changes of aging. However, the individualization of type 2 myocardial infarction within acute myocardial lesions was not obvious, nor was the impact on mortality, which was essentially based on the burden of comorbidities
2

Atoui, Rony R. "Marrow stromal cells as "universal donor cells" for myocardial regenerative therapy." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101837.

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Background. Recently rodent and porcine bone marrow stromal cells (MSCs) have been reported to be uniquely immune tolerant. In order to confirm these findings in human cells, we tested the hypothesis that human MSCs are also immune tolerant, such that they can be useful as "universal donor cells" for myocardial regenerative therapy.
Methods. Immunocompetent female rats underwent left coronary ligations (n=90). They were randomized into 3 groups. In Group I, lac-Z labeled male human MSCs were implanted into the peri-infarcted area. In Group II and III isogenic rat MSCs or culture medium were injected respectively. Echocardiography was carried out to assess cardiac function, and the specimens were examined serially for up to 8 weeks with immunohistochemistry, FISH and PCR to examine MSCs survival and differentiation.
Results. Human MSCs were found to survive within the rat myocardium without immunosuppression. This was confirmed by PCR and FISH test. No cellular infiltration characteristic of immune rejection was noted. Some of these cells appeared to express cardiomyocyte-specific markers such as troponin-Ic and connexin-43. Furthermore, the implanted MSCs significantly contributed to the improvement in ventricular function and attenuated LV remodeling.
Conclusions. Human MSC survived within this xenogeneic environment, and contributed to the improvement in cardiac function. Our findings support the feasibility of using these cells as "universal donor cells" for xeno- or allo-geneic cell therapy, as they can be tested, prepared and stored well in advance for urgent use. Allogeneic MSCs from healthy donors may be particularly useful for severely ill or elderly patients whose own MSCs could be dysfunctional.
Plusieurs études ont récemment démontré la tolérance immunologiquedes cellules souches stromales (CSS) issues de rongeurs et de porcinés. Pour confirmer cesrésultats chez les cellules humaines, l'étude actuelle évalue l'effet des CSS humaines sur larégénération du myocarde chez des rats immunocompétents et étudie la possibilité d'utiliserces CSS comme « donatrices universelles» à la suite d'un infarctus.
3

Legallois, Damien. "Paramètres biologiques et échocardiographiques et remodelage ventriculaire gauche après syndrome coronarien aigu avec sus-décalage du segment ST Definition of left ventricular remodelling following ST-elevation myocardial infarction: a systematic review of cardiac magnetic resonance studies in the past decade Left atrial strain quantified after myocardial infarction is associated with ventricular remodeling The relationship between circulating biomarkers and left ventricular remodeling after myocardial infarction: an updated review Serum neprilysin levels are associated with myocardial stunning after ST-elevation myocardial infarction Is plasma level of Coenzyme Q10 a predictive marker for left ventricular remodeling after revascularization for ST-segment elevation myocardial infarction ?" Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC429.

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Le remodelage ventriculaire gauche est une complication fréquente des patients ayantprésenté un syndrome coronarien aigu, pouvant conduire à terme à une situation d’insuffisancecardiaque. Il est donc important de connaître les facteurs associés à la survenue d’un remodelageventriculaire afin de dépister plus précocement les patients à plus haut risque d’insuffisance cardiaqueet ainsi optimiser leur prise en charge. Ce travail comprend deux axes. Le premier porte sur larecherche de nouveaux paramètres d’imagerie associés à la survenue du remodelage. Nous avonsdans un premier temps réalisé une revue de la littérature concernant la définition du remodelageventriculaire gauche en imagerie par résonance magnétique. Puis, nous avons conduit deux étudesayant pour but de rechercher une association entre (i) le strain atrial gauche et, (ii) le gradient depression intraventriculaire gauche diastolique, évalués en échocardiographie 24-48 heures après lesyndrome coronarien aigu et le remodelage ventriculaire gauche au cours du suivi. Le second axe portesur les biomarqueurs associés au remodelage ventriculaire post-infarctus. Nous avons réalisé une revuede la littérature au sujet des biomarqueurs qui, dosés lors de l’hospitalisation initiale, sont associés àl’existence d’un remodelage lors du suivi. Nous avons ensuite étudié la valeur prédictrice de deuxbiomarqueurs (la néprilysine et le coenzyme Q10) pour la survenue d’un remodelage ventriculairegauche
Left ventricular remodeling is a common complication in patients following acutemyocardial infarction and may lead to heart failure. Some baseline parameters are associated withremodeling at follow-up, allowing to better discriminate patients with an increased risk of heart failureto optimize therapeutics. This work has two axes, focused on imaging and biological parametersassociated with left ventricular remodeling, respectively. First, we reviewed past studies that definedremodeling using cardiac magnetic resonance imaging. Then, we studied the association betweensome echocardiographic parameters (left atrial strain and diastolic intraventricular pressure gradient)and left ventricular remodeling after ST-elevation myocardial infarction. In the other axis, wereviewed biomarkers that have been associated with left ventricular remodeling in prior studies. Then,we investigated the association between neprilysin and coenzyme Q10 levels and left ventricularremodeling in STEMI patients

Книги з теми "Universal definition of myocardial infarction":

1

Thygesen, Kristian, Joseph S. Alpert, Allan S. Jaffe, and Harvey D. White. The universal definition of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0041.

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Myocardial infarction is defined pathologically as myocyte necrosis due to prolonged ischaemia. These conditions are met when there is a detection of a rise and/or fall of cardiac biomarkers, preferably troponins, with at least one value above the 99th percentile of the upper reference limit, together with evidence of myocardial ischaemia, as recognized by at least one of the following: symptoms of ischaemia, electrocardiographic changes of new ischaemia, the development of pathological Q waves, imaging evidence of a new loss of viable myocardium or new regional wall motion abnormality, or the identification of an intracoronary thrombus by angiography or autopsy.
2

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.

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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
3

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.

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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
4

Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.

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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
5

Price, Susanna, Roxy Senior, and Bogdan A. Popescu. Acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0062.

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Echocardiography is fundamental to the assessment and management of patients with acute cardiac disease, and differs from outpatient echocardiography in some key areas. Echocardiography provides important information throughout the whole patient pathway, having been shown to change interventions in 60–80% patients in the pre-hospital setting, improve diagnostic accuracy and efficiency in the emergency room, and reveal the aetiology of unexplained hypotension in 48% of medical intensive care patients. Echocardiography is now included in the universal definition of acute myocardial infarction, and in international guidelines regarding the management of cardiac arrest. In the critical care setting, echocardiography can be used to as a haemodynamic monitor, to determine abnormalities of cardiac physiology and coronary perfusion, as well as defining the underlying cardiac diagnosis. This chapter focuses on situations relevant to acute cardiac care, however, where discussed elsewhere in this textbook (acute coronary syndromes, pulmonary embolism, takotsubo, aortic disease, pericarditis, cardiomyopathies, heart failure, and valvular disease) they are not covered in detail here.
6

Arntz, Hans-Richard. Sudden cardiac death: epidemiology and prevention. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0005.

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Even if sudden cardiac death is considered to be the most frequent cause of death in adults in industrialized countries, its incidence varies widely, depending on the definition and the source and quality of underlying data. It is estimated that about 70-80% of cases are due to coronary heart disease. The remaining 20% are attributable to a wide variety of inborn, genetically determined or acquired diseases, including a small group with hitherto undefined background. Prevention primarily encompasses the treatment of cardiovascular risk factors to avoid manifestations of coronary heart disease. Furthermore, preventive strategies are targeted to define groups of patients with an increased risk for sudden cardiac death or individuals at risk in specific populations, e.g. competitive athletes. A major target group are patients with impaired left ventricular function, preferentially due to myocardial infarction. These patients, and some less clearly defined patient groups with non-ischaemic cardiomyopathy and heart failure, may benefit from the insertion of an implantable cardioverter-defibrillator. With regard to pharmacological prevention, treatment of the underlying condition is the mainstay, since no antiarrhythmic substance-with the exemption of beta-blockers in some situations-has shown to be of efficacy.

Частини книг з теми "Universal definition of myocardial infarction":

1

Vahanian, Alec, and Robert Ferrari. "Universal Definition of Myocardial Infarction." In Compendium of Abridged ESC Guidelines 2010, 307–12. Tarporley: Springer Healthcare Ltd., 2010. http://dx.doi.org/10.1007/978-1-907673-10-8_21.

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2

Thygesen, Kristian, Joseph Alpert, and Harvey White. "Universal Definition of Myocardial Infarction 2007." In Compendium of Abridged ESC Guidelines 2011, 297–302. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-31-9_21.

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3

Thygesen, Kristian, Joseph S. Alpert, Allan S. Jaffe, and Harvey D. White. "The universal definition of myocardial infarction." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 463–78. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0038.

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Myocardial infarction is defined by the presence of myocardial injury detected by abnormal cardiac biomarkers in the setting of acute clinical myocardial ischaemia. These conditions are met when there is a detection of a rise and/or fall of cardiac biomarkers, preferably cardiac troponins, with at least one value above the 99th percentile of the upper reference limit together with evidence of acute clinical myocardial ischaemia as recognized by at least one of the following: symptoms of ischaemia, ECG changes of new ischaemia, development of pathological Q waves, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality, or identification of an intracoronary thrombus by angiography or autopsy.
4

Thygesen, Kristian, Joseph S. Alpert, Allan S. Jaffe, and Harvey D. White. "Chapter 39 The universal definition of myocardial infarction." In The ESC Textbook of Intensive and Acute Cardiac Care. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199584314.003.0041.

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5

Thygesen, Kristian, Joseph Alpert, and Allan Jaffe. "The Definition of Myocardial Infarction." In Clinical Guide to Primary Angioplasty, 40–46. CRC Press, 2010. http://dx.doi.org/10.3109/9781841847351-5.

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6

Alpert, Joseph S., Kristian Thygesen, Allan S. Jaffe, and Harvey D. White. "Terminology of acute coronary syndromes and definition of myocardial infarction." In Coronary Care Manual, 19–24. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-7295-3927-2.10004-1.

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7

Ramrakha, Punit S., Kevin P. Moore, and Amir Sam. "Cardiac emergencies." In Oxford Handbook of Acute Medicine, 1–164. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199230921.003.01.

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Adult basic life support 4 Adult advanced life support 6 Universal treatment algorithm 8 Acute coronary syndrome (ACS) 10 ST elevation myocardial infarction (STEMI) 12 STEMI: diagnosis 1 14 STEMI: diagnosis 2 16 STEMI: general measures 18 STEMI: reperfusion therapy (thrombolysis) 1 20 STEMI: thrombolysis 2 ...
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Kumar, Preetham, M. Khalid Mojadidi, Jonathan M. Tobis, Bernhard Meier, and David Thaler. "Definition of Cryptogenic Stroke, the RoPE Score, and Assessment of Embolic Stroke of Undetermined Source." In Patent Foramen Ovale Closure for Stroke, Myocardial Infarction, Peripheral Embolism, Migraine, and Hypoxemia, 45–55. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-816966-7.00004-x.

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Ramrakha, Punit S., Kevin P. Moore, and Amir H. Sam. "Cardiac emergencies." In Oxford Handbook of Acute Medicine, 1–170. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198797425.003.0001.

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This chapter describes cardiac emergencies, including adult life support (basic and advanced), universal treatment algorithm, acute coronary syndrome (ACS), ST-elevation myocardial infarction (STEMI; diagnosis, general measures, reperfusion therapy, thrombolysis, reperfusion by primary percutaneous coronary intervention (PCI), surgery, predischarge risk stratification, complications), ventricular septal defect post-myocardial infarction (MI), atrial tachyarrhythmia post-MI, bradyarrhythmias and indications for pacing, hypotension and shock post-MI, cardiogenic shock, non-ST-elevation MI (NSTEMI; diagnosis, risk stratification, medical management, invasive and non-invasive strategies, discharge, and secondary prevention), arrhythmias, tachyarrhythmias, tachycardia (broad complex, monomorphic, polymorphic, ventricular, narrow complex), atrial fibrillation (AF), atrial flutter, multifocal atrial tachycardia (MAT), accessory pathway tachycardia, atriventricular nodal re-entry tachycardia (AVNRT), bradyarrhythmias, sinus bradycardia, intraventricular conduction disturbances, pulmonary oedema, endocarditis (infective, culture-negative, right-sided, prosthetic valve, prophylaxis), acute aortic regurgitation (AR), acute mitral regurgitation (MR), deep vein thrombosis (DVT), pulmonary embolism (PE), fat embolism, hypertensive emergencies, hypertensive encephalopathy, aortic dissection, acute pericarditis, bacterial pericarditis, cardiac tamponade, and congenital heart disease in adults.
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Waldmann, Carl, Andrew Rhodes, Neil Soni, and Jonathan Handy. "Haematological drugs." In Oxford Desk Reference: Critical Care, 235–43. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198723561.003.0015.

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This chapter discusses haematological drugs and includes discussion on anticoagulants and heparin-induced thrombocytopenia (including unfractionated heparin, low-molecular weight heparins, danaparoid, coumarins, synthetic pentasaccharides, the direct oral anticoagulants, and thromboprophylaxis in critical care patients), thrombolysis (definition of thrombolysis, physiology of fibrinolysis, contraindications to thrombolysis, factors influencing a successful outcome, myocardial infarction, acute limb ischaemia, and pulmonary embolism), and antifibrinolytics (describing the efficacy of tranexamic acid in reducing traumatic bleeding, the efficacy of tranexamic acid in reducing surgical bleeding, and the efficacy of tranexamic acid in postpartum haemorrhage).

Тези доповідей конференцій з теми "Universal definition of myocardial infarction":

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Chapman, Andrew, Philip Adamson, Anoop Shah, Atul Anand, Fiona Strachan, Kuan Ken Lee, Amy Ferry, et al. "144 High-sensitivity cardiac troponin and the fourth universal definition of myocardial infarction." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.141.

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Hinton, Jonathan, Maclyn Augustine, Lavinia Gabara, Mark Mariathas, Rick Allan, Florina Borca, Zoe Nicholas, et al. "37 Incidence and one year outcome of periprocedural myocardial infarction following cardiac surgery: are the universal definition and scai criteria fit for purpose?" In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.37.

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Julian, D. G. "UNSTABLE ANGINA : DEFINITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643709.

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A satisfactory definition of unstable angina continues to be elusive.Like stable angina, it is a clinicalsyndrome, and mustbe defined in those terms. In both cases, it is understood that myocardial ischaemiabut not infarction is responsible for the symptoms. For angina to earn the “unstable” label, theremust have been the recent development or deterioration of symptoms. Traditionally, “recent” has meant within the last month, but it has become increasingly clear thatthe time frame is of critical importance - the patient with a sudden irruption of severe chest pain in the last two days is likely to have a different pathology and prognosis from the individual who first developed exercise-induced pain two weeks ago, which has not worsened during this period. Likewise, the patient who hadhis last attack of pain one week agois very different from one who had his last attack one hour ago; indeed in the HINT study, there was a high incidence of myocardial infarction undetected on admission in the lattergroup (Br Heart J 1986;56:400-13).A problem that has hardly been addressed is “When does unstable angina stop being unstable?”. The answer must be when it either becomes stable (i.e. stops getting worse),or proceeds to myocardial infarctionor death.Most studies have shown that the vast majority of patients stablise quickly, often losing their symptoms completely. There is, however, a group of patients who fail to respond promptly to medical treatment, and it isthese patients who are most likely to go on to angiography, angioscopy, angioplasty, surgery, myocardial infarction or death. Thus, the enormously valuable information we have obtained from, for example, angiography and necropsy studies applies essentially only to this subset of unstableangina patients, albeit they are themost severe. Unfortunately, such studies tell us relatively little aboutthe more dynamic aspects of the disorder, such as the role of coronary vasomotion.It is only relatively recently that clinicians have appreciated that they have quite simple means of suspecting the mechanisms involved. Thus, the history of progressive exercise-induced angina on the one hand or angina only at rest on theother must tell us something of the underlying physiopathology. Likewise,the fact that the symptoms respond to rest, or beta-blockers, or calcium antagonists also provides evidenceas to causation.Thus, while all would agree that angina is “unstable” whenit has recently developed or worsened, it must bediscussed in subsetsdefined by their history and response to treatment.In this way, we may be able to assign a patient to a particular clinicalgroup, which will indicate that it is likely that he has a particular physiopathology, which inturn will suggest the most appropriate management.
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AlMukdad, Sawsan Ibrahim, Hazem Elewa, and Daoud Al-Badriyeh. "Economic Evaluation of CYP2C19 Genotype-Guided Antiplatelet Therapy Compared to Universal use of Ticagrelor or Clopidogrel in Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0170.

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Background: Patients having CYP2C19 loss-of-function alleles and receiving clopidogrel are at higher risk of adverse cardiovascular outcomes. Ticagrelor is a more effective and expensive antiplatelet that is unaffected by the CYP2C19 polymorphism. The main aim of the current research is to evaluate the cost-effectiveness among CYP2C19 genotype-guided therapy, universal ticagrelor, and universal clopidogrel after a percutaneous coronary intervention (PCI). Methods: A two-part simulation model, including a one-year decision-analytic model and a 20-year followup Markov model, was created to follow the use of (i) universal clopidogrel, (ii) universal ticagrelor, and (iii) genotype-guided antiplatelet therapy. Outcome measures were the incremental cost-effectiveness ratio (ICER, cost/success) and incremental cost-utility ratio (ICUR, cost/qualityadjusted life years [QALY]). Therapy success was defined as survival without myocardial infarction, stroke, cardiovascular death, stent thrombosis, and no therapy discontinuation because of adverse events, i.e. major bleeding and dyspnea. The model was based on a multivariate analysis, and a sensitivity analysis confirmed the robustness of the model outcomes. Results: Against universal clopidogrel, genotype-guided therapy was cost-effective over the one-year duration (ICER, USD 6,102 /success), and dominant over the long-term. Genotype-guided therapy was dominant over universal ticagrelor over the one-year duration and cost-effective over the long term (ICUR, USD 1,383 /QALY). Universal clopidogrel was dominant over ticagrelor over the short term, and cost-effective over the long-term (ICUR, 10,616 /QALY). Conclusion: CYP2C19 genotype-guided therapy appears to be the preferred antiplatelet strategy, followed by universal clopidogrel, and then universal ticagrelor for post-PCI patients in Qatar.

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